High dose antipsychotic polypharmacy and dopamine partial agonists - time to rethink guidelines?

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@firemonkey , do you understand the medical terminology in all those articles you are posting so many times. Or any other on this forum may understand it.

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In order to make the pharmaceutical researches reach ideal treatment at the highest level for dangerous side effects that arise from the influence of the psychotic factor on the cognitive aspect and the chemical background associated to it
At first,you must know the ID of the psychotic factor (disorder maker ), its functional characteristics and the mechanism of effect

For example,Why the change (the main disorder) in the chemical background does not occur inside the neuron cell but outside between the neuron cells ?
Why the chemical disorder (no matter what is it )and cognitive change occurs after the transmission not before or during ?
if the wrong in the thought’s data, transmitter or /transmission pathway /or in the receptor or reception process Or in the processes that is supposed to happen after the reception ?

They said "Dopamine is one of the neurotransmitters found at the level of the synaptic space, space in-between neurons. Dopamine is released in the synaptic space from vesicles housed in the pre-synaptic neuron, then binds to dopamine receptors at the level of the postsynaptic neuron. Think of this as a key and lock type of effect where dopamine receptors are locks that open when the dopamine “key” enters the lock.

In the case,if the increase in the amount of dopamine that is self-excreted is the cause that is creates the whole sz condition or its symptoms (according to the hypothesis)

Treating this amount by closing the receptors Completely or Partially does not achieve the recovery from the sz condition in the youth age or any period of time !

The effect of medical intervention have no effect on the psychotic factor, rather,it is effects on things irrelevant the condition or/functional cause or its mechanism who is produces the mental ,emotional and behavioral bad side symptoms ,and in all cases it does not induce enough treatment to return the mind or self-knowledge data to its original state before the sz occurrence

Is this not enough to believe that the transmitters or receptors from A to Z are not the creation cause of sz condition or the cause of its bad side effects (negative,positive and cognitive symptoms ) ?